eMedicine Specialties > Gastroenterology > Systemic Disease

Upper Gastrointestinal Bleeding

Author: Maurice A Cerulli, MD, FACG, Chief, Division of Gastroenterology and Hepatology, Associate Professor of Clinical Medicine, Department of Internal Medicine, Division of Gastroenterology, New York Methodist Hospital, Cornell University
Coauthor(s): Shahzad Iqbal, MD, Advanced Endoscopy Fellow, Department of Gastroenterology, Columbia University Medical Center
Contributor Information and Disclosures

Updated: Nov 20, 2009

Introduction

Background

The diagnosis and therapy for nonvariceal upper gastrointestinal bleeding (UGIB) has evolved over the past 3 decades from passive diagnostic esophagogastroduodenoscopy with medical therapy until surgical intervention was needed to active intervention with endoscopic techniques followed by angiographic and surgical approaches if endoscopic therapy failed. Variceal hemorrhage is not discussed in this article because the underlying mechanisms of bleeding are different and require different therapies.

The underlying mechanisms of nonvariceal bleeding involve either arterial hemorrhage, such as in ulcer disease and mucosal deep tears, or low-pressure venous hemorrhage, as in telangiectasias and angioectasias. In variceal hemorrhage, the underlying pathophysiology is due to elevated portal pressure transmitted to esophageal and gastric varices and resulting in portal gastropathy. (See images below and Images 1, 5, 7.)

Ulcer with a clean base.

Ulcer with a clean base.

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Ulcer with a clean base.

Ulcer with a clean base.


Ulcer with a visible vessel.

Ulcer with a visible vessel.

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Ulcer with a visible vessel.

Ulcer with a visible vessel.


Ulcer with active bleeding.

Ulcer with active bleeding.

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Ulcer with active bleeding.

Ulcer with active bleeding.


The patient presents with an ulcer that has bled or is actively bleeding. Approximately 80% of ulcers stop bleeding. The overall mortality rate is approximately 10%. This patient population has become progressively older, with significant comorbidities that increase mortality. Rebleeding or continued bleeding is associated with increased mortality; therefore, differentiating the patient with a low probability of rebleeding and little comorbidity from the patient at high risk for rebleeding with serious comorbidities is imperative.

In the early history of endoscopy for UGIB, multiple published studies questioned the cost-effectiveness of endoscopy in this setting because it was unclear whether the outcome was changed. In a setting in which 80% of patients respond to conservative medical management, studies were hampered by type 2 errors because of the large number of patients needed to demonstrate statistical significance. Much debate also focused on the significance of the nonbleeding visible vessel (ie, color, size, diagnostic characteristics, risk of rebleeding) in ulcer hemorrhage. These matters became clarified after the characteristics and the significance of the visible vessel in the ulcer crater were defined and the evidence for endoscopic therapy was established, demonstrating that patients requiring therapy to control bleeding or rebleeding could be diagnosed and treated at the time of the upper endoscopy.

In 1989, a National Institutes of Health consensus conference on UGIB concluded that effective therapy was needed in the presence of active bleeding or a visible vessel. The consensus conference affirmed that the treatment, when performed by an experienced endoscopist using 1 of 4 techniques (ie, injection of epinephrine or sclerosants, heater-probe coagulation, bipolar electrode coagulation, laser coagulation), was proven effective by the published evidence. Three other techniques have since been developed: (1) endoscopic application of clips, (2) use of banding devices, and (3) argon plasma coagulation.

Emergency surgery typically entails oversewing the bleeding vessel in the stomach or duodenum (usually preoperatively identified by endoscopy), vagotomy with pyloroplasty, or partial gastrectomy. Angiographic obliteration of the bleeding vessel is considered in patients with poor prognoses.

Other causes of gastrointestinal bleeding include mucosal tears in the esophagus or upper stomach due to vomiting (Mallory-Weiss tears), venous blebs, or vascular ectasias. These lesions can be treated with endoscopic coagulation. The bleeding from gastric cancers and ulcers in leiomyomas does not usually respond to endoscopic therapy; surgical or radiologic intervention is needed.

Pathophysiology

Duodenal ulcer disease is strongly associated with Helicobacter pylori infection. The organism causes disruption of the mucous barrier and has a direct inflammatory effect on gastric and duodenal mucosa. Eradication of H pylori has been demonstrated to reduce the risk of recurrent ulcers and, thus, recurrent ulcer hemorrhage.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are the second major etiology of ulcer hemorrhage because of their effect on cyclooxygenase-1, which leads to impaired mucosal defense to acid.1 The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer hemorrhage, although only when not combined with aspirin therapy. Concerns have been raised about an increase in myocardial infarction and stroke in patients taking selective cyclooxygenase-2 inhibitors. As demonstrated in the study by al-Assi et al, the combination of H pylori infection and NSAID use may increase the risk of ulcer hemorrhage; however, the treatment of H pylori in patients who are taking NSAIDs remains controversial.2

As the ulcer burrows deeper into the gastroduodenal mucosa, the process causes weakening and necrosis of the arterial wall, leading to the development of a pseudoaneurysm. The weakened wall ruptures, producing hemorrhage. The flow through the vessel varies with the fourth power of the radius; thus, small increases in vessel size can mean much larger amounts of blood flow and bleeding. Visible vessels usually range from 0.3-1.8 mm.

Exsanguinating hemorrhage has been reported from larger vessels. The larger vessels are located deeper in the gastric and duodenal submucosa and serosa. Larger branches of the left gastric artery are found high on the lesser curvature, while the pancreatoduodenal artery and its major branches are located posteroinferiorly in the duodenal bulb. The size of the vessel is important in the prognosis in that larger vessels cause faster blood loss, with more severe hypotension and more complications, especially in older patients.

During vomiting, the lower esophagus and upper stomach are forcibly inverted. Vomiting attributable to any cause can lead to a mucosal tear of the lower esophagus or upper stomach. The depth of the tear determines the severity of the bleeding. Rarely, vomiting can result in esophageal rupture (Boerhaave syndrome), leading to bleeding, mediastinal air entry, left pleural effusion (salivary amylase can be present) or left pulmonary infiltrate, and subcutaneous emphysema.

Gastric cancer is an uncommon cause of hemorrhage in the United States, but it remains a major problem in non-Western countries; worldwide, it is the leading cause of digestive cancer deaths. Patients with chronic liver disease and portal hypertension are at increased risk for variceal hemorrhage and portal gastropathy in addition to ulcer hemorrhage.

Frequency

United States

UGIB is a common medical condition that results in high patient mortality and medical care costs. Annually, approximately 100,000 patients are admitted to US hospitals for therapy for UGIB. Peptic ulcer disease is the most common cause of UGIB.3 However, the proportion of cases caused by peptic ulcer disease has declined.4 The decrease is believed to be due to the use of proton pump inhibitors (PPIs) and H pylori therapy.

International

UGIB is a common occurrence throughout the world. In France, a report concludes that the mortality from UGIB has decreased from about 11% to 7%; however, a similar report from Greece finds no decrease in mortality. In a nationwide study from Spain, UGIB was 6 times more common than lower GI bleeding.5

Mortality/Morbidity

Patients typically present with an ulcer that has bled or is actively bleeding, but approximately 80% of ulcers stop bleeding. The overall mortality rate is approximately 10%. In a retrospective chart review by Yavorski RT et al, 73.2% of deaths occurred in patients older than 60 years.6 In patients with UGIB, comorbid illness and not actual bleeding is the major cause of death. Comorbid illness was noted in 50.9% of patients, with similar occurrence in males (48.7%) and females (55.4%). One or more comorbid illnesses were noted in 98.3% of patients who died, and, in 72.3% of patients, comorbid illnesses were the primary cause of death.1,6

According to the American Society for Gastrointestinal Endoscopy (ASGE), the following risk factors are associated with increased mortality, recurrent bleeding, the need for endoscopic hemostasis, or surgery: age older than 60 years, severe comorbidity, active bleeding (eg, witnessed hematemesis, red blood per nasogastric tube, fresh blood per rectum), hypotension, red blood cell transfusion greater than or equal to 6 units, inpatient at time of bleed, and severe coagulopathy.7

An increasing amount of evidence in the literature states that therapy with high-dose PPIs (IV bolus followed by continuous infusion) may decrease the rate of rebleeding after endoscopic therapy. By increasing the gastric pH above 6, the clot is stabilized.

Sex

The incidence of UGIB is 2-fold greater in males than in females, in all age groups; however, the death rate is similar in both sexes.6

Age

This patient population has become progressively older, with significant comorbidities that increase mortality. As mentioned above, the mortality increases with older age (>60 y) in both males and females.8

Clinical

History

  • The patient history findings include weakness, dizziness, syncope associated with hematemesis (coffee ground vomitus), melena (black stools with a rotten odor), and hematochezia (red or maroon stool).
  • Patients may have a history of previous dyspepsia (especially nocturnal symptoms), ulcer disease, early satiety, and nonsteroidal anti-inflammatory drug or aspirin use. Many patients with UGIB who are taking nonsteroidal anti-inflammatory drugs present without dyspepsia but with hematemesis or melena as their first symptom. Low-dose aspirin (81 mg) has been associated with UGIB with or without the addition of NSAID therapy. Patients with a prior history of ulcers are at an especially increased risk for UGIB when placed on aspirin or NSAID therapy and should receive continuous acid suppression with a PPI.
  • Because recurrence of ulcer disease is common, history findings are relevant.
    • Patients may present in a more subacute phase with a history of dyspepsia and occult intestinal bleeding manifesting as a positive fecal occult blood test result or as iron deficiency anemia.
    • A history of recent aspirin ingestion suggests that the patient may have nonsteroidal anti-inflammatory drug gastropathy with an enhanced bleeding diathesis from poor platelet adhesiveness.
    • A history of chronic alcohol use of more than 50 g/d or chronic hepatitis (B or C) increases the risk of variceal hemorrhage, gastric antral vascular ectasia (GAVE), or portal gastropathy.
    • The presence of postural hypotension indicates more rapid and severe blood loss.

Physical

  • The goal of the patient's physical examination is to evaluate for shock and blood loss.
    • Pulse and blood pressure should be checked with the patient in supine and upright positions to note the effect of blood loss. Significant changes in vital signs with postural changes indicate an acute blood loss of approximately 20% or more.
    • Other signs of shock include cool extremities, oliguria, chest pain, presyncope, confusion, and delirium.
    • Hematemesis and melena should be noted. The redder the stool, the more rapid the transit, which suggests a large upper tract hemorrhage.
  • Signs of chronic liver disease should be noted, including spider angiomata, gynecomastia, increased luneals, splenomegaly, ascites, pedal edema, and asterixis.
  • Signs of tumor are uncommon but portend a poor prognosis. Signs include a nodular liver, abdominal mass, and enlarged and firm lymph nodes.
  • The finding of subcutaneous emphysema with a history of vomiting is suggestive of Boerhaave syndrome (esophageal perforation) and requires prompt consideration of surgical therapy.
  • The finding of telangiectasias may indicate the rare case of Osler-Weber-Rendu syndrome.

Causes

  • The major causes of UGIB are duodenal ulcer hemorrhage (25%), gastric ulcer hemorrhage (20%), mucosal tears of the esophagus or fundus (Mallory-Weiss tear), esophageal varices, erosive gastritis, erosive esophagitis, Dieulafoy lesion, gastric varices, gastric cancer, and ulcerated gastric leiomyoma.
  • Rare causes of UGIB include aortoenteric fistula, gastric antral vascular ectasia, angiectasias, and Osler-Weber-Rendu syndrome.
  • The proportion of UGIB cases caused by peptic ulcer disease has declined.4 This decline is believed to be due to the use of PPIs and H pylori therapy.
  • Patients should be considered for upper endoscopy if blood loss from the upper gastrointestinal tract is suspected. A high level of suspicion of UGIB should exist when the patient has a history of intake of aspirin or NSAID, even if no history of hematemesis or melena exists. The color of stool containing blood depends on the transit time; rapid transit from the upper gastrointestinal tract can result in red or maroon stools. Melena results from more than 100 mL of blood with moderate transit time. Slow transit of blood from the lower intestine can result in melena in the presence of obstruction.
  • Urgent endoscopy is indicated when patients present with hematemesis, melena, or postural changes in blood pressure. Cooper et al have demonstrated a lower rate of rebleeding and shorter length of stay when endoscopy is performed within 24 hours of admission.9,10
  • Primary surgical intervention should be considered in patients with a perforated viscus (eg, from perforated duodenal ulcer, perforated gastric ulcer, or Boerhaave syndrome). In patients who are poor operative candidates, conservative treatment with nasogastric suction and broad-spectrum antibiotics can be instituted. Endoscopic clipping or sewing techniques have also been used in such patients.

More on Upper Gastrointestinal Bleeding

Overview: Upper Gastrointestinal Bleeding
Differential Diagnoses & Workup: Upper Gastrointestinal Bleeding
Treatment & Medication: Upper Gastrointestinal Bleeding
Follow-up: Upper Gastrointestinal Bleeding
Multimedia: Upper Gastrointestinal Bleeding
References
Further Reading
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Keywords

upper gastrointestinal bleeding, gastrointestinal bleeding, peptic ulcer, stomach ulcer, duodenal ulcer, upper GI bleeding, esophageal varices, bleeding ulcer, gastric ulcer, gastric cancer, gastric varices, UGIB, gastrointestinal disease, GI hemorrhage, upper endoscopy, infection, infection, erosive gastritis, erosive esophagitis, Dieulafoy lesion, Osler-Weber-Rendu syndrome

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Contributor Information and Disclosures

Author

Maurice A Cerulli, MD, FACG, Chief, Division of Gastroenterology and Hepatology, Associate Professor of Clinical Medicine, Department of Internal Medicine, Division of Gastroenterology, New York Methodist Hospital, Cornell University
Maurice A Cerulli, MD, FACG is a member of the following medical societies: American College of Gastroenterology, American Gastroenterological Association, American Medical Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Coauthor(s)

Shahzad Iqbal, MD, Advanced Endoscopy Fellow, Department of Gastroenterology, Columbia University Medical Center
Shahzad Iqbal, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society of Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Medical Editor

Alex Jacocks, MD, Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Douglas M Heuman, MD, FACP, FACG, AGAF, Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA, Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital
John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract
Disclosure: AMGEN Royalty Other

 
 
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